Hypothalamic Control Of Eating

Question 0

What are the short term signals of satiety?

Answer 0

1. Oropharyngeal
   - taste
2. Gastric infusion (stretch of the GI)
   -Nutrient value has no effect in stomach
   However nutrient value in the intestine has effect as well as stretch
3. Post absorptive satiety (liver)
   Glucose and free FAs –> decreased intake

Question 1

Why do we stop eating?

Answer 1

Satiety factors from GI tract (CCK) –> vagus –> hypothalamus all short term

Long term
Fat –> leptin

Question 2

Where does short term satiety info go in the stomach?

Answer 2

Stomach –> stretch mechanoreceptors –> vagal afferents –> NTS of medulla –> decrease ipfood intake

Get same firing rate

Question 3

What hormone is released in the duodenum and what does it do?

Answer 3

CCK –> gall bladder contraction–> bile release –> fate metabolism
CCK –> pyloric constriction + gastric contractions –> increase in stomach activity –> digestion
CCK –> receptors of vagal afferents mechanoreceptors (same as stretch) –> increase activity in NTS –> decrease food intake

Question 4

What hormone is released from the stomach and is increased by fasting?

Answer 4

Ghrelin

Major affect is orexigenic –> increase apatite

Question 5

What is Pradee-Willi syndrome?

Answer 5

1:25000

Symptoms: fetal hypotonia, mental retardation, hypogonadotropic hypogonadism (decreased FSH and LH)
Obesity by hyperplasia (exessive eating)
By hyper ghrelin secretion

Question 6

What is the source of leptin?

Answer 6

Ob gene, made by adipose cells

Question 7

What does leptin do?

Answer 7

Decreased food intake

Question 8

What happens in obesity with relation to leptin?

Answer 8

Receptor insensitivity

Question 9

Where does leptin act in the brain?

Answer 9

Brainstem–> NTS
Hypothalamus

Increase responsiveness to gastric stretch

Question 10

What effect does leptin have of the stomach?

Answer 10

Increases gastric sensitivity to stretch by acting in the solitary nucleus

Question 11

What is the Lateral hypothalamic area (LHA) do?

Answer 11

Lesion causes aphagia (no eating) by damage to MFB –> reduced motivation to eat (meso-limbic system DA)

OR damage to MFB –> reduced motor function

Aphagia due to loss of neurons that synthesize orexigenic

Activation of LHA –> orexin –> eating

Question 12

What does the PVN do?

Answer 12

Releases oxytocin and vasopressin
ALSO –> NTS –> stim causes decrease in eating

Releases catabolic (decrease eating and growth) 
--> CRH --> in brainstem causes less eating

Question 13

What does the Arcuate nucleus do?

Answer 13

Integrates the PVN and LHA

Question 14

What are the two populations in the ARC?

Answer 14

1st –> neuropeptide Y –> PVN and LHA –> more eating

2nd –> melanocortin (POMC) –> PVN and LHA
–> less food intake

Question 15

What does leptin do to the hypothalamus?

Answer 15

Inhibits ARC NPY neurons and decrease food intake

Activates ARC melanocortin and decreases food intake

Question 16

Where does ghrelin act? And what does it do?

Answer 16

Acts in the ARC

Increases NPY neuronal activity and increases food intake